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The primary FRCA structured oral exam

MEDICINE

Study Guide 1
Second Edition
Packed with new guidelines and current hot topics, this book and its companion
The Primary FRCA Structured Oral Examination Study Guide 2 are the
definitive revision aids to the Primary FRCA structured oral examination. This
second edition is revised and updated in line with the new Royal College of
Anaesthetists guide, with eight new sections to reflect changes to the RCA’s
model questions and a major revision of six of the existing sections.
Features


Comprehensive resource to prepare for the SOE



Aligned to the Royal College of Anaesthetists Guide




Summary diagrams and flowcharts effectively distil the key points

About the Authors
Lara Wijayasiri and Kate McCombe are both Consultant Anaesthetists at
Frimley Health NHS Trust

K28792

an informa business

6000 Broken Sound Parkway, NW
Suite 300, Boca Raton, FL 33487
711 Third Avenue
New York, NY 10017
2 Park Square, Milton Park
Abingdon, Oxon OX14 4RN, UK

ISBN: 978-1-78523-098-1

90000
9 78 1 785 23098 1

w w w. c rc p r e s s . c o m

Wijayasiri & McCombe

Authors Kate McCombe and Lara Wijayasiri wrote the first edition when they
were trainees, after failing to find a good resource to prepare for the SOE
component of the FRCA Primary exam. They wanted a book that contained
model answers to the RCA’s published model questions – this book provided,
and continues to provide, just that.

The Primary FRCA Structured Oral Examintion Study Guide 1 • Second Edition

The Primary FRCA
Structured Oral
Examination

The Primary FRCA
Structured Oral
Examination Study Guide 1
Second Edition
Lara Wijayasiri and Kate McCombe
Illustrations by Paul Hatton • Foreword by David Bogod


The Primary FRCA
Structured Oral
Examination Study Guide 1
Second Edition

Lara Wijayasiri and Kate McCombe
Illustrations by Paul Hatton • Foreword by David Bogod

Boca Raton London New York

CRC Press is an imprint of the
Taylor & Francis Group, an informa business

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CRC Press
Taylor & Francis Group
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Boca Raton, FL 33487-2742
© 2016 by Taylor & Francis Group, LLC
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Version Date: 20160307
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contents
Forewordv
Prefacevii
Contributorsix
Acknowledgementxi

PART 01
PHYSIOLOGY1
1. Red blood cells and haemoglobin
2
2. Oxygen–haemoglobin dissociation curve
4
3. Hypoxia
7
4. Oxygen transport
12
5. Carbon dioxide transport
15
6. Alveolar gas equation . .
18
7. Ventilation–perfusion (V /Q ) mismatch and shunt
20
8. Respiratory dead space
25
9. Lung volumes
28
10. Lung compliance
31
11. Control of respiration
34
12. Altitude and diving
39
13. Lung function measurement
44
14. Effects of anaesthesia on lung function
48
15. Baroreceptors and control of blood pressure
50
16. Cardiac cycle
53
17. Coronary circulation
54
18. Exercise
56
19. Carbohydrate metabolism
58
20. Starvation
63
21. Nausea and vomiting
66
22. Liver physiology
68
23. Gastric regulation
72
24. Total parenteral nutrition
75
25. Acid–base balance
78
26. Buffers
81
27. Renal blood flow
85
28. Glomerular filtration rate
87
29. Renal handling of glucose, sodium and inulin
91
30. Fluid compartments
93
31. Osmoregulation
97
32. Action potentials
99
33. Cerebral blood flow
102
34. Cerebrospinal fluid
106
35. Autonomic nervous system
109
36. Child versus adult
112
37. Pregnancy
114

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CONTENTS
38. Placental transfer
39. Fetal circulation
40. Ageing
41. Adrenal gland
42. Thyroid gland
43. Eye
44. Endothelium
45. Portal circulations
46. Immune mechanisms
47. Pain pathways
48. Muscle electrophysiology
49. Reflexes

116
118
120
122
124
126
127
129
131
134
140
142

PART 02
PHYSICS145
50. Definitions
146
51. Standard international units
150
52. Principles of measurement
152
53. Gas laws
157
54. Supply of medical gases
160
55. General aspects of pressure
164
56. Pressure regulators
166
57. Flow
169
58. Electrical components
172
59. Defibrillators
175
60. Electrical safety
177
61. Diathermy
180
62. States of matter, heat capacity and latent heat
182
63. Temperature measurement
189
64. Pollution and scavenging
193
65. Oxygen measurement
196
66. pH measurement
200
67. Carbon dioxide measurement
202
68. Blood pressure measurement
204
69. Arterial pressure waveform
207
70. Cardiac output monitoring
210
71. Depth of anaesthesia monitoring
217
72. Safety features of the anaesthetic machine
220
73. Disconnection monitors
223
74. Breathing systems
225
75. Resuscitation bags and valves
230
76. Ventilators
234
77. Vaporisers
237
78. Neuromuscular blockade monitoring
244
79. Lasers
251
80. Ultrasound and Doppler
254
81. CT and MRI
257
82. Pulse oximetry
260
Index263

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Foreword
Much has happened since I wrote the Foreword to the first edition of this invaluable guide
to the Primary FRCA Structured Oral Examination in 2010. Of the three original authors, two
have married (each other) and produced a baby girl. One of these two has had to relinquish
the authorship of this new edition, since his promotion to the ranks of Primary Examiner
unsurprisingly bars him from writing a book on how to pass the Primary exam. The two
remaining authors have both moved up the ranks and been appointed as consultants,
one with an interest in obstetrics, ethics and law, and the other specialising in vascular
anaesthesia and the difficult airway. The first edition, meanwhile, has rapidly become the
best-selling textbook on the Primary SOE. If a soap opera was ever to be based around the
publication of a guide to passing post-graduate anaesthetic exams – admittedly an unlikely
proposition – the story of McCombe and Wijayasiri would surely rival ‘EastEnders’ for
intrigue and plot development.
In this new edition, as well as updating existing topics, the authors have included substantial
additions to what was already a very comprehensive book, in line with changes made by
the Royal College to the Primary syllabus. The section on ‘special patient groups’ now
includes paediatrics and the elderly, the latter of increasingly personal interest to this writer.
The section on physics – often a stumbling block for the Primary candidate – has been
extensively revised and now covers those perennial favourites of the examiners, arterial
waveforms and vaporisers; as one reads these, there are frequent ‘aha!’ moments, not
least with respect to critical damping, the pumping effect and the influence of altitude on
performance. Mindful of the old adage that ‘a picture paints a thousand words’, the authors
have enhanced the number and quality of diagrams and figures, helping to clarify areas such
as fetal circulation and the Kreb’s cycle.
Some aspects of these books remain, thankfully, unchanged, in particular the resolutely
pragmatic approach that McCombe and Wijayasiri take to help readers through the tangled
thickets of the Primary. Here are the questions the examiners like to ask, the authors
seem to say, and this is how to answer them. It is, perhaps, a tribute to the exam syllabus
itself that this approach results in a textbook that is not only very readable but also highly
educational.
In short, if you are not lucky enough to be working in the same hospital as the authors, and
you cannot approach them for viva practice (or even if you can), then the new edition of this
book is an essential companion and a true vade mecum. Look it up – a bit of Latin can still
impress the examiners!
David Bogod
Consultant Anaesthetist and Ex-Editor-in-Chief of Anaesthesia
Nottingham

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PREFACE
During our revision for the primary exam we were advised that the best way to ensure
success in the structured oral examination (SOE) was to prepare answers to all of the
questions in the back of The Royal College of Anaesthetists Guide to the FRCA Examination,
The Primary. Undoubtedly, this was excellent advice but it proved an enormous task and
one we simply did not have time to complete before our own exams. However, once they
were over, we began to answer all those questions in the hope that this might help others to
prepare for the Primary, or for the basic science component of the Final FRCA. Finally, then,
here is the result: the book we wish we’d had.
The Primary FRCA Structured Oral Examination Study Guide provides answers to the
questions regularly posed by the examiners. We have not attempted to write the next
great anaesthetic textbook, but rather to collate information and deliver it in a relevant and
userfriendly layout to make your exam preparation a little easier.
In the SOE itself, each topic will be examined for approximately five minutes. Many of
these answers contain much more information than could reasonably be expected of you
in that time; however, we have tried to cover several angles of questioning.
We have included the usual chapters on physiology, physics (Study Guide 1) and
pharmacology (Study Guide 2) and, in addition, have written a section on patients who
present the anaesthetist with unique problems, ‘special patient groups’ (Study Guide 2).
These patients tend to appear in the clinical SOE before some terrible ‘critical incident’
befalls them. Again, we have included a section addressing the ‘critical incidents’ beloved of
the examiner, with advice as to how to approach them in the SOE (Study Guide 2).
There is a unique pharmacology section including information on drugs commonly examined
presented in a spider diagram layout. These extremely visual learning aids allowed us to
revise the drugs in the necessary detail, and helped us to recall the information even under
the acute stress of the exam. We hope you find them just as useful.
We wish you every success in what is undoubtedly a rigorous exam. We believe the key to
this success is to practise presenting the knowledge that you already have, logically and
concisely. The only way to do this is to practise speaking, even though the possibility of
exposing any ignorance is daunting. The more you talk, the more you will cover, and every
question is so much easier to answer in the exam if you have already had a dress rehearsal.
We hope this book will help you in your preparations.
Good luck!
Lara Wijayasiri
Kate McCombe
December 2015

vii
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To Andrew, who makes me believe anything is possible.
Kate McCombe
To Amish, my husband and best friend- thank you for giving me the time to complete this
book. And to Maya, my beautiful daughter- thank you for giving me a greater focus in life
other than this book.
Lara Wijayasiri

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Contributors
Paul Hatton B.Tec
Illustrations
Dr Barbara Lattuca MBBCh MRCP FRCA
Locum Consultant Anaesthetist, St George’s NHS Healthcare Trust
Physiology
>
>
>
>
>
>
>
>
>
>

Acid-base balance
Buffers
Renal blood flow
Glomerular filtration rate
Renal handling of glucose, sodium, inulin
Fluid Compartments
Osmoregulation
Baroreceptors
Immune mechanisms
Pain pathways

Lt Col Mark Wyldbore MBBS BSc(Hons) FRCA RAMC
Consultant Anaesthetist, Queen Victoria Hospital NHS Foundation Trust
Physiology
> Reflexes

Physics
>
>
>
>
>
>

General aspects of pressure
Pressure regulators
Electrical components
Defibrillators
Electrical safety
Diathermy

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Acknowledgement
Dr Tim Case MBBChir MPhil MA(Cantab)
Our sincerest thanks go to Tim for his eagle eyes and enviable grasp of physics. The book is
better for his meticulous reading and attention to detail!

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Part

01

PHYSIOLOGY

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01 PHYSIOLOGY PHYSIOLOGY

1. Red blood cells
and haemoglobin
How are red blood cells (RBCs)
produced?

The process of RBC production is called erythropoiesis.
Production of RBCs is controlled by erythropoietin, a hormone produced in
the kidneys.
RBCs start as immature cells in the red bone marrow and after about seven
days of maturation they are released into the bloodstream. The stages of
RBC formation are:
Proerythroblast → Prorubricyte → Rubricyte → Normoblast →
Reticulocyte (nucleus ejected by this phase, allowing the centre of the cell to indent
giving the cell its biconcave shape – these now squeeze out of the bone marrow and
into the circulation) → Erythroblast

Hypoxia (e.g. altitude or anaemia) stimulates the kidney to release more
erythropoietin, which acts on the red bone marrow where it increases the
speed of reticulocyte formation.
How are worn out RBCs removed
from the circulation?

RBCs survive for about 120 days. Their cell membranes are exposed to a
lot of wear and tear as they squeeze through blood capillaries. Without a
nucleus and other organelles, RBCs cannot synthesise new components.
Worn out RBCs are removed from the circulation and destroyed by fixed
phagocytic macrophages in the spleen and the liver and the breakdown
products are recycled.

What happens to the breakdown
products of RBCs?

Haemoglobin gets split into its haem and globin components – the globin
is broken down into amino acids and the haem gets broken down into iron
and biliverdin. The iron combines with the plasma protein transferrin, which
transports the iron in the bloodstream. In the muscle, liver and spleen, iron
detaches from transferrin and combines with iron-storing proteins – ferritin
and haemosiderin. When iron is released from its storage site or absorbed
from the gut, it combines with transferrin and gets transported to the bone
marrow where it is used for RBC production. Biliverdin gets converted into
bilirubin, which enters the circulation and is transported to the liver where
it is secreted into the bile.

Why is haemoglobin essential?

Oxygen is relatively insoluble in water and therefore only approximately 1.5%
of total oxygen is carried dissolved in the plasma. The remaining 98.5% is
bound to haemoglobin. Haemoglobin increases the oxygen-carrying capacity
of blood approximately 70-fold.

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RED BLOOD CELLS AND HAEMOGLOBIN

Describe the molecular structure
of haemoglobin.

The haemoglobin molecule is a tetramer composed of four subunits. Each
subunit consists of a polypeptide chain (globin) in association with a haem
group. A haem group consists of a central charged iron atom held in a ring
structure called a porphyrin.
Different forms of haemoglobin exist depending on the structure of these
polypeptide chains. In normal adults 98% of all haemoglobin is in the form of
HbA1 (2 α chains and 2 β chains). The remaining 2% is in the form of HbA2
(2 α chains and 2 δ chains). Fetal haemoglobin (HbF) is composed of 2 α
chains and 2 γ chains. HbF changes to HbA at around six months of life.

What happens to haemoglobin
in sickle cell anaemia?

Sickle cell anaemia is an inherited autosomal recessive blood disorder in
which there is an abnormal β polypeptide chain due to a genetic mutation
in the amino acid sequence where the amino acid valine is replaced
by glutamic acid. In the heterozygous state this confers an advantage
against malaria as the shortened lifespan of the erythrocyte prevents the
blood-borne phase of the mosquito from completing its life cycle. In the
homozygous state the abnormal haemoglobin is susceptible to forming
solid, non-pliable sickle-like structures when exposed to low PaO2, causing
the erythrocytes to obstruct the microcirculation, leading to painful crises
and infarcts.

What happens to haemoglobin
in thalassaemia?

Thalassaemia is an inherited autosomal recessive blood disorder in which
the genetic defect results in a reduced rate of synthesis of one of the
globin chains that make up haemoglobin. This can result in the formation of
abnormal haemoglobin molecules, causing anaemia. Thalassaemia can be
α or β depending on which globin chain is being underproduced.
Thalassaemia is a quantitative problem where too few globin chains are
synthesised, whereas sickle cell anaemia is a qualitative problem with the
synthesis of an incorrectly functioning globin chain.

How does oxygen bind to
haemoglobin?

Oxygen binds to the ferrous iron (Fe2+) in haemoglobin by forming a
reversible bond. There is no oxidative reaction and so the iron atom always
remains in the ferrous form. In the condition methaemoglobinaemia, the
ferrous iron is oxidised into the ferric (Fe3+) form.
Each molecule of haemoglobin can bind four molecules of oxygen (i.e. one
at each ferrous ion within each haem group). There are several factors that
influence binding including local oxygen tension, local tissue environment
(temperature, CO2, hydrogen ions and 2,3 DPG) and the allosteric change
and cooperative binding behaviour of oxygen to haemoglobin (see
Chapter 2, ‘Oxygen–haemoglobin dissociation curve’, for further details).

Can the dissolved fraction of
oxygen be dismissed?

Even though dissolved oxygen represents a small fraction of total oxygencarrying capacity of the blood, it still constitutes an important fraction.
Severe anaemia illustrates the point, e.g. for a Jehovah’s Witness who has
experienced a massive intra-operative haemorrhage and refuses blood
transfusion. One therapeutic option would be the use of hyperbaric oxygen
therapy; at three atmospheres and using 100% oxygen the dissolved fraction
of oxygen would meet total body oxygen requirements.
The dissolved fraction of oxygen is also responsible for triggering the hypoxic
respiratory drive. This is of clinical significance in patients with COPD who
are chronic CO2 retainers, because giving them high-flow oxygen to increase
their PaO2 may lead to loss of their hypoxic drive.
In 2008, the British Thoracic Society published guidelines on the use of
emergency oxygen in adults. The guidelines recommend that oxygen be
administered to patients whose oxygen saturations fall below the target
range (94–98% for most acutely ill patients and 88–92% for those at risk of
type 2 respiratory failure with raised CO2 levels in the blood).

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01 PHYSIOLOGY

2. Oxygen–haemoglobin
dissociation curve
Draw the oxygen–haemoglobin
dissociation curve (OHDC).

The OHDC is a graph relating the percentage of haemoglobin saturated with
oxygen to the partial pressure of oxygen (PO2).

Arterial

100

Venous

% Saturation

75

50

P50

0
3.5

5.3

13.3
PO2 (kPa)

Fig. 2.1  The oxygen–haemoglobin dissociation curve

Normal oxyhaemoglobin
dissociation curve

> Arterial PO2 is 13.3 kPa with a Hb saturation of 97% (it is not 100% due to
venous admixture constituting physiological shunt).
> Venous PO2 is 5.3 kPa with a Hb saturation of 75%.
> P50 is 3.5 kPa (this is the PO2 at which Hb is 50% saturated and it is the
conventional point used to compare the oxygen affinity of Hb).

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OXYGEN–HAEMOGLOBIN DISSOCIATION CURVE

Explain the shape of the OHDC.

The OHDC has a characteristic sigmoid shape due to the binding
characteristics of haemoglobin to oxygen:
> Allosteric modulation 
When oxygen binds to haemoglobin, the two β chains move closer together
and change the position of the haem moieties that assume a ‘relaxed’ or R
state. When oxygen dissociates from haemoglobin, the reverse happens and
the haem moieties take up a ‘tense’ or T state.
> Cooperative binding 
When oxygen binds to haemoglobin the R state is favoured, which has
an increased affinity for oxygen and so facilitates the uptake of additional
oxygen. The affinity of haemoglobin for the fourth oxygen molecule is,
therefore, much greater than that for the first.

What are the major physiological
factors that determine the
position of the OHDC?

>Factors that shift the OHDC to the right: This facilitates the unloading
of oxygen into tissues and the P50 value is higher than 3.5 kPa:
• ↓ pH
• ↑ Temperature
• ↑ 2,3-Diphosphoglycerate
• ↑ PaCO2
• HbS
• Anaemia
• Pregnancy
• Post-acclimatisation to altitude.
>Factors that shift the OHDC to the left: This facilitates the uptake of
oxygen from the lungs and the P50 value is lower than 3.5 kPa:









↑ pH
↓ Temperature
↓ 2,3-Diphosphoglycerate
↓ PaCO2
HbF
Methaemoglobin
Carboxyhaemoglobin
Stored blood.

What is the Bohr effect?

This describes the right shift in the OHDC in association with increased
PaCO2 and hydrogen ion concentration.

What is the double Bohr effect?

This refers to the situation in the placenta where the Bohr effect operates in
both the maternal and fetal circulations. The increase in PCO2 in the maternal
intervillous sinuses assists oxygen unloading. The decrease in PCO2 on the
fetal side of the circulation assists oxygen loading. The Bohr effect facilitates
the reciprocal exchange of oxygen for carbon dioxide. The double Bohr
effect means that the oxygen dissociation curves for maternal HbA and fetal
HbF move apart − i.e. right shift (maternal); left shift (fetal).

What is the Haldane effect?

This describes the increased ability of deoxygenated haemoglobin to carry
carbon dioxide. Conversely, oxygenated blood has a reduced capacity to
carry carbon dioxide. The Haldane effect occurs because deoxygenated
haemoglobin is a better proton acceptor than oxyhaemoglobin.

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01 PHYSIOLOGY
How does the OHDC compare
with the myoglobin dissociation
curve?

Myoglobin is an oxygen-carrying protein found in skeletal muscles
(it gives muscle its dark red appearance).
It consists of a single polypeptide chain associated with a haem moiety.
Unlike haemoglobin, it can only bind one molecule of oxygen and, therefore,
its dissociation curve is a rectangular hyperbola.
Myoglobin also has a higher affinity for oxygen than haemoglobin, and so its
dissociation curve lies to the left of the OHDC.
Myoglobin takes up oxygen from the circulating haemoglobin and releases
it into exercising muscle tissues at very low PO2, thus providing a source of
oxygen during periods of sustained muscle contractions when blood flow to
these muscles may be constricted due to blood vessel compression.

100

Myoglobin

% Saturation

Haemoglobin

50

P50

P50

0.13

3.5
PO2 (kPa)

Fig. 2.2  Myoglobin dissociation curve compared to oxyhaemoglobin dissociation curve

6
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HYPOXIA

3. Hypoxia
Hypoxia is a core respiratory physiology question and as such examiners will expect a thorough understanding of this
topic. Structure your answer.
Define hypoxia and classify the
causes.

Hypoxia may be defined either as an inadequate oxygen supply or the
inability to utilise oxygen at a cellular level. Causes are divided into four
main types:
> Hypoxic hypoxia – a PaO2 < 12 kPa
• Low FiO2, e.g. inadvertent hypoxic gas delivery during anaesthesia
• Hypoventilation, e.g. opiate induced
• Diffusion impairment, e.g. pulmonary oedema, pulmonary fibrosis
• Ventilation–perfusion mismatch, e.g. COPD, asthma, LRTI
• Shunt, e.g. atelectasis causing intrapulmonary shunt
>
Anaemic hypoxia – normal PaO2 but inadequate oxygen-carrying
capacity
• Low circulating haemoglobin level, e.g. acute and chronic anaemias
• Normal circulating haemoglobin level but reduced ability to carry
oxygen, e.g. carbon monoxide poisoning
>
Stagnant hypoxia – normal PaO2 and oxygen-carrying capacity but
reduced tissue and organ perfusion
• e.g. cardiogenic shock
>
Histotoxic hypoxia – normal PaO2, oxygen-carrying capacity and tissue
perfusion but an inability of the tissues to utilise the oxygen at a cellular
mitochondrial level
• e.g. cyanide poisoning

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01 PHYSIOLOGY
Draw oxyhaemoglobin dissociation curves showing arterial (♦);
and mixed venous (•); points in
the four types of hypoxia.

Arterial

100

Venous

% Saturation

75

P50

50

0
3.5

5.3

13.3
PO2 (kPa)

Fig. 3.1  Normal oxyhaemoglobin dissociation curve

> Arterial PaO2 13.3 kPa.
> Venous Pv– O2 5.3 kPa.
>P50 3.5 kPa (partial pressure of oxygen at which haemoglobin is 50%
saturated).

100

% Saturation

Arterial

50

Venous

3.5

7.2
PO2 (kPa)

Fig. 3.2  Oxyhaemoglobin dissociation curve in hypoxic hypoxia

>PaO2 is reduced.
>Pv– O2 is reduced with venous desaturation (<75%).

8
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HYPOXIA

% Saturation

100

50

13.3

3.5

PO2 (kPa)
Fig. 3.3  Oxyhaemoglobin dissociation curve in anaemic hypoxia

> PaO2 remains normal (>13.3 kPa).
> Global oxygen delivery is reduced due to reduced oxygen content.
> Result is increased oxygen extraction and venous desaturation.

100

% Saturation

75

13.3

5.3
PO2 (kPa)

Fig. 3.4  Oxyhaemoglobin dissociation curve in stagnant hypoxia

> PaO2 is normal.
> Pv– O2 is normal.
> Tissues and organs do not receive the oxygenated blood due to
perfusion failure.

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01 PHYSIOLOGY

% Saturation

100

75

8.0

13.3

PO2 (kPa)
Fig. 3.5  Oxyhaemoglobin dissociation curve in histotoxic hypoxia

> PaO2 is normal.
> Cells are unable to utilise oxygen resulting in high venous saturations.
> Cyanide poisoning will also be associated with a left shift of the
oxyhaemoglobin dissociation curve.
What is oxygen content?

Oxygen is carried in the blood in two main ways: combined with
haemoglobin and dissolved in the plasma. Oxygen content is calculated
by combining the proportion of oxygen bound to haemoglobin with that
dissolved.



Oxygen content = [Bound Oxygen] + [Dissolved Oxygen]
= [Hb · 1.34 · SaO2] + [PaO2 · 0.0225]

Where:
Hb
Haemoglobin g/dL
1.34Huffner’s constant – each gram of haemoglobin combines with
1.34 mL oxygen
SaO2Arterial oxygen saturation as a percentage, e.g. 96% = 0.96
PaO2
Partial pressure of arterial oxygen
0.0225 mL of oxygen per dL per kPa of oxygen partial pressure
Thus oxygen content may be calculated for arterial (CaO2) and venous
(Cv– O2) blood.
E.g. In arterial blood: Hb 15 g/dL, SaO2 100% and PaO2 13.3 kPa
Arterial oxygen content = [15 · 1.34 · 1.0] + [13.3 · 0.0225]

= [20.1] + [0.3]

= 20.4 mL of oxygen per dL

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HYPOXIA
E.g. In venous blood: Hb 15 g/dL, Sv– O2 75% and Pv– O2 5.3 kPa
Venous oxygen content  = [15 · 1.34 · 0.75] + [5.3 · 0.0225]

= [15] + [0.2]

= 15.2 mL of oxygen per dL
Note that the difference between arterial and venous oxygen content is just
under 5 mL of oxygen per dL. If oxygen content is multiplied by cardiac
output, oxygen delivery is obtained.
If circulating volume for a 70 kg man is 80 mL/kg (5600 mL), this equates
to an arterial oxygen content of just over 1000 mL and a venous oxygen
content of approximately 750 mL.
Discuss arterial and venous
oxygen content in the four types
of hypoxia.

Hypoxic hypoxia
E.g. Altitude: Hb 15 g/dL , SaO2 85%, PaO2 6.5 kPa, Pv– O2 3.0 kPa,
Sv– O2 45%
CaO2 = [15 · 1.34 · 0.85] + [6.5 · 0.0225] = 17 mL O2/dL
Cv– O2 = [15 · 1.34 · 0.45] + [3.0 · 0.0225] = 9 mL O2/dL
Note arterial oxygen content is reduced and there is increased oxygen
extraction resulting in a lower venous oxygen content.
Anaemic hypoxia
E.g. Haemorrhage: Hb 7 g/dL, SaO2 100%, PaO2 13.3 kPa, Pv– O2 4.0 kPa,
Sv– O2 50%
CaO2 = [7 · 1.34 · 1.0] + [13.3 · 0.0225] = 10 mL O2/dL
Cv– O2 = [7 · 1.34 · 0.5] + [4.0 · 00225] = 5 mL O2/dL
Significant reduction in arterial oxygen content and hence oxygen delivery to
the tissues. There will be a resultant increase in cardiac work in an attempt to
maintain oxygen delivery to the tissues.
Stagnant hypoxia
E.g. Cardiogenic shock: Hb 15 g/dL, SaO2 100%,  PaO2 13.3 kPa, Pv– O2 5.3,
Sv– O2 75%
CaO2 = [15 · 1.34 · 1.0] + [13.3 · 0.0225] = 20 mL O2/dL
Cv– O2 = [15 · 1.34 · 0.75] + [5.3 · 0.0225] = 15 mL O2/dL
Note arterial oxygen content is normal. However, circulatory dysfunction
results in inadequate oxygen delivery to organs and venous saturations may
even be increased.
Histotoxic hypoxia
E.g. Cyanide poisoning: Hb 15 g/dL, SaO2 100%, PaO2 13.3 kPa, Pv– O2
8.0 kPa, Sv– O2 90%
CaO2 = [15 · 1.34 · 1.0] + [13.3 · 0.0225] = 20 mL O2/dL
Cv– O2 = [15 · 1.34 · 0.9] + [8.0 · 0.0225] = 18 mL O2/dL
Arterial oxygen content is normal. However, at a cellular level there is an
inability to utilise oxygen, resulting in high venous oxygen content. This
picture may also be seen in severe sepsis where despite adequate oxygen
delivery cellular hypoxia remains with high central venous saturations.

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01 PHYSIOLOGY

4. Oxygen transport
Oxygen transport is a fundamental respiratory physiology question and examiners will expect complete
understanding of the topic.
How is oxygen transported from
the lungs to the cells of the
tissues?

> Ventilation of the lungs supplies oxygen to the alveolus.
>Diffusion of oxygen across the alveolus to the pulmonary capillaries.
>Oxygen carriage by blood (combined with haemoglobin and dissolved in
plasma).
>Diffusion from capillary to mitochondria.

What is the oxygen cascade?

The oxygen cascade describes the sequential reduction in PO2 from
atmosphere to cellular mitochondria.
Humidification

Mixing with alveolar gas

13.8

13.3
Arterial
Blood
6–7
Capillary
Blood

Pasteur Point

Atmosphere

A-a gradient

15
Alveolar Gas Equation
PAO2 = PIO2 – PACO2/RQ

0.3

20
Gas humidified at 37 °C
(101.3 – 6.3) x 0.21

PO2
(kPa)

Mixing with dead space gases
Inspired dry gas: (101.3 kPa x 0.21)

21

1– 2
Mitochondria
Mitochondria

Fig. 4.1  The oxygen cascade

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